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Diagnosis and Management of Acute Ischemic Stroke
DOI: http://dx.doi.org/10.5772/.106389
Figure 3.
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A rat model of the effect of decreased cerebral blood flow (CBF; measured in mL/100g/min) on neuronal
physiology and brain tissue. Below 15mL/100g/min, ATP is depleted, Na/K pumps fail, and cells die, forming the
ischemic core. Below 35mL/100g/min, there is a change in neuronal metabolism and the neuron is not conducting
action potentials. The tissue is non-functional but has not infarcted yet. This is the ischemic penumbra, the region
that is still salvageable by intervention and “doomed to die” without it. Below 55mL/100g/min, the tissue is “at
risk” but will not necessarily die, even without intervention. Adapted from lieu et al. 2020.
Measurement parameter Core Penumbra
Mean Transit Time (MTT)
T Max
Cerebral Blood Flow (CBF)
Cerebral Blood Volume (CBV)
Table 2 .
CT perfusion measurements for core and penumbra. In both the core and the penumbra, due to blockage of the
artery, there is less flow of blood to the tissue, leading to decreased CBF. The blood is also taking longer to fill
and to leave the tissue and therefore, MTT and T max are increased. In the core infarct, cerebral blood volume is
decreased as blood is no longer filling the dead tissue.
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The penumbra can be determined by subtracting the ischemic core from the
tissue at risk There have been multiple methods of estimating the tissue-at-risk or
the perfusion deficit as well as estimating the ischemic core. Visually, comparing
MTT maps to CBV maps gives a qualitative estimate of the penumbra (Figure ).
The most useful quantitative measurements are Tmax>6s, which best estimates
tissue-at-risk and CBF<30ml/100g/min, which best estimates core [40]. One
can also calculate the MMR, which is the ratio between the core volume and
perfusion deficit volume. These numbers are crucial as they determine eligibility
for endovascular thrombectomy. To be eligible for the intervention, the MMR
must be greater than 1.8, the penumbra must be greater than 15mL, and the Tmax
>10seconds [41].
There are caveats pertaining to potential inaccuracy of the above parameters.
CTP parameters may be affected by reduced cardiac output, carotid artery stenosis,
and injection rate. Technical factors such as motion artifacts, and erroneous CTP
protocol, for example wrong contrast injection rate, can also bias the computation of
ischemic core and penumbra [39]. A perfusion protocol shorter than 60seconds, as a
further example, is known to overestimate the infarct core volume [30]. Occasionally
CTP results can be entirely misleading when a non-stroke hemisphere is labeled as
ischemic due to recanalization and luxury hyperperfusion of the stroked hemisphere
[42]. Stroke mimics causing vascular dysregulation, such as seizures, hypertensive
encephalopathy, hemiplegic migraines, may produce false images of penumbra,
and so can vascular anatomical variations [39]. Although CTP has become standard
in assessing anterior circulation stroke, there is to date insufficient evidence for its
application in posterior circulation strokes. In particular, the CBF cut off of 30%,
a defining feature of the ischemic core, can only be applied to anterior circulation
strokes. MRI on the other hand is considered the gold standard for assessing posterior circulation infarcts [43].
Figure 4.
CT perfusion map of a patient with acute left MCA occlusion with mean transit time map (MTT; left) and
cerebral blood volume map (CBV; right) demonstrating acute occlusion of left MCA. In the MTT map, increased
time is indicated by a color higher on the spectrum with the longest time being red. It can be seen that the region
marked by the white arrow has a prolonged MTT versus the right hemisphere. On the CBV map, the color lower
on the spectrum demonstrates lower CBV.
Diagnosis and Management of Acute Ischemic Stroke
DOI: http://dx.doi.org/10.5772/.106389
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Magnetic resonance imaging (MRI) and diffusion weighted imaging
(DWI)- fluid attenuated inversion recovery (FLAIR) mismatch
Another method of determining mismatch is by using magnetic resonance
imaging (MRI). This is a newer, more sensitive form of imaging compared to CT. Its
primary advantages are its high spatial resolution and versatility in use. Its main disadvantages are that the images take longer than CT to acquire and the scanners are not
nearly as common or accessible as for CT. Nevertheless, specific MRI sequences can
provide crucial information for the diagnosis of AIS. A diffusion-weighted imaging
(DWI) measures the diffusion of water molecules across the cellular membrane [44].
In patients with AIS, due to disruption of the electrochemical gradient, this diffusion
is disrupted. This shows up at hyperintense or bright on imaging. This bright signal
can be detected for at least 2 weeks after the initial event [45]. The apparent diffusion coefficient (ADC) image is the inverse of the DWI and has low intensity during
this period. The DWI and ADC image are useful in demonstrating whether there is
any ischemia to a region, reversible or irreversible. The T2 fluid attenuated inversion
recovery (FLAIR) image is the sequence that is used to see the structure and anatomy
of the brain tissue. In the hyperacute phase, the FLAIR has variable intensity and
increases in intensity after 6hours. The FLAIR image demonstrates structural damage
and irreversible infarcted tissue [44]. To be a candidate for endovascular thrombectomy, the DWI volume must be greater than 70mL [40]. In situations of uncertain
onset, positive DWI with negative FLAIR, known as a DWI-FLAIR mismatch,
strongly suggest that the stroke is hyperacute and there is significant mismatch
(Figure ). Using DWI-FLAIR mismatch, once can predict if an AIS is presenting
within 4·5h of LKNT with 62% (95% CI: 57–67) sensitivity, 78% (95% CI: 72–84)
specificity, 83% (95% CI: 79–88) positive predictive value, and 54% (95% CI: 48–60)
negative predictive value [46]. Therefore, in patients in whom LKNT is unknown,
MRI DWI-FLAIR mismatch can be used to identify patients who would still remain
candidates for thrombolysis, which will be discussed in detail later [47].
There are a plethora of other MR sequences and techniques that can be used in
the diagnosis and management of AIS. Susceptibility weighted imaging (SWI) is a
sequence that is sensitive to products that especially distort the magnetic field like
iron. Given blood breakdown products contain iron, SWI provides information about
the existence of possible hemorrhagic transformation has occurred within the first
12hours [25, 48]. MR angiography without contrast (time-of-flight) is an alternative
to CT angiography [49]. And MR perfusion has obtained 90% concordance between
CT-based and MR-based mismatch status [40], and is a highly reliable alternative for
patients not amenable to NCCT and CTA.
. Emergent bloodwork
Emergent laboratory investigations should include complete blood count, elec-
trolytes, aPTT, INR, creatinine, and glucose [7]. It is not necessary to wait for all the
results before thrombolysis, as blood glucose can be reliably given by a finger stick
test, and as mentioned, creatinine values are not needed prior to performing CTA.
Other labs such as an INR>1.7, platelets <100,000/mm3, and blood glucose <50mg/
dL, are also helpful as they are part of the relative contraindications for tPA, discussed
in further detail later. Patients suspected of having ischemic strokes should have a
12-lead EKG and initiate telemetry. This may assess cardiac rhythm and uncover atrial
fibrillation [50].
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. Treatment of acute ischemic stroke
. Introduction
As discussed in the previous section, the prompt recognition of AIS using physical
exam and its diagnosis using non-contrast CT (NCCT), CT-angiography (CTA), and
CT Perfusion (CTP) is the first step in the efficient and effective management. In the
last two decades, we have learned much about the treatment of AIS beginning with
the concept of the “ischemic penumbra” to the use of thrombolysis in AIS and finally,
to the revolutionary procedure of mechanical thrombectomy.
. Principles of treatment
As mentioned previously, there exists an ischemic penumbra in patients with AIS,
tissue that is at risk but that has not yet infarcted. The primary goal of AIS management is to use interventions to recanalize the occluded artery and restore perfusion to
the penumbra [38]. These interventions and these patients must be selected carefully
to maximize benefit and avoid harm. In the following section, these interventions and
the selection process will be discussed.
. Thrombolysis
One of the methods of recanalizing the occluded artery is by breaking up the
thrombus using intravenous pharmacotherapy. Thrombi that occlude intracerebral
arteries are created when the protein fibrin creates strands of protein that are long
and insoluble [51]. The insoluble protein binds to platelets and the cross-linked
fibrin forms a mesh over the platelet-protein complex forming a plug. Thrombolytic/
fibrinolytic drugs such as alteplase, or tissue-plasminogen activator (tPA) cleave
the inactive protein plasminogen into its active form plasmin. Plasmin degrades
the fibrin matrix that was reinforcing the thrombus, thereby allowing clot break
down and recanalization. In 1995, the landmark NINDS trial [15] demonstrated that
patients with AIS that received tPA within 3 hours of patient LKNT had a significantly higher likelihood of favorable outcome (39%) at 3 month follow-up compared
to those who received placebo (26%) as measured by the Modified Rankin Scale
(Odds ratio: 1.7). However, there was also a significantly higher risk of symptomatic
intracerebral hemorrhage (ICH; Table ) in the tPA group (6.4%) versus the placebo
group (0.6%). It was not until 2008 “European Cooperative Acute Stroke Study”
(ECASS) III trial [52], that the tPA window was extended to 4.5hours. A subsequent
systematic review of four clinical trials investigating thrombolysis [55] determined
that, as the time to symptom onset increases, the benefit from tPA declines and the
risk of mortality increases. Beyond the 4.5hour window, the risk of tPA outweighs
the benefits (Figure ). In a metanalysis of 6756 patients from nine studies [56], the
authors found that patients who received tPA and a 5.55% increase in absolute risk
of parenchymal type II hematoma [54] (Odds ratio: 5.55), 3.1% increase in absolute
risk of SITS-MOST ICH (Odds ratio: 6.67), and 2.3% increase in absolute risk of fatal
ICH (Odds ratio: 7.14). One of the main caveats of thrombolysis is that the clinician
must know the patient’s LKNT. There are a significant proportion of patients that in
whom the time of symptom onset is unknown. Traditionally, these patients would
not be candidates for thrombolysis as the benefit-to-risk ratio would not be known.
However, the landmark WAKE-UP trial, investigated the use of thrombolysis in this
Diagnosis and Management of Acute Ischemic Stroke
DOI: http://dx.doi.org/10.5772/.106389
Study Definition of symptomatic ICH
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NINDS Any new ICH on NCCT associated with any neurologic deterioration [15]
ECASS III If associated with neurological decline of an increase of ≥4 points on the NIHSS [52]
SITS-MOST Parenchymal hematoma type 2* on imaging 22–36hours after intervention with
*
A hematoma which occupies or more of the infarcted tissue and is accompanied with obvious mass effect on
adjacent tissue [].
Table 3 .
Different definitions of symptomatic ICH depending on clinical trial [47]. The NINDS trial used the most liberal
definition, explaining the higher estimates of ICH compared to what was reported in subsequent studies.
neurological deterioration of ≥4 points on NIHSS [53]
group of patients [47]. The authors used MRI with diffusion to determine if there
was still a significant volume of penumbra and mismatch, and in carefully selected
patients, thrombolysis was administered. There was a greater likelihood of favorable
outcome in patients administered tPA (53.3%) versus those who received placebo
(41.8%) at 3 months (Odds ratio: 1.61). In the DIAS trial, the authors used a highly
fibrin-specific thrombolytic agent, desmoteplase, in patients presenting with AIS
[57]. The patients presented between 3 and 9hours from LKNT and were carefully
selected by use of MRI to determine who would be a good candidate for thrombolysis. A higher rate of reperfusion and favorable outcome was seen in patients who
were given thrombolysis (71.4% and 60.0%) compared with those who received placebo (19.2% and 22.2%). Therefore, if a center does have MRI capabilities, carefully
selected patients with AIS with unknown time of symptom onset may be candidates
for thrombolysis.
Table shows the indications and contraindications for thrombolysis for patients
presenting with AIS [7]. The only absolute contraindication to administration of
thrombolysis is demonstration of ICH on NCCT. The other criteria listed are relative
and are dependent on the clinical situation. For a patient to be a candidate for thrombolysis, the stroke should be classified as clinically disabling, usually referring to a
NIHSS>5
2
. The “Phase IIIB, Double-Blind, Multicenter Study to Evaluate the Efficacy
and Safety of Alteplase in Patients With Mild Stroke: Rapidly Improving Symptoms
and Minor Neurologic Deficits” (PRISMS) trial compared administration of tPA to
aspirin in patients with AIS presenting with a NIHSS≤5 and determined that there
was no significant difference in favorable outcome at 3 months [58].
Once it is determined that a patient is a candidate for thrombolysis, the dosing
should be calculated, and formulation prepared. The dose that is primarily used for
AIS is 0.9mg/kg of patient’s ideal body weight, with a maximum dose of 90mg [7].
Of the total dose, 10% is administered as a bolus over 1minute and the remainder
as an infusion over 60minutes. The ENCHANTED trial investigated a lower dose
of tPA, 0.6mg/kg in a cohort of Asian patients presenting with AIS and although
they demonstrated a lower risk of ICH compared to standard dose (1% vs. 2.1%),
the trial was not able to show noninferiority of the lower dose with respect to death
or disability at 3 months [59]. While alteplase is standard of care for thrombolysis
in AIS, in the last 10 years, there is evidence suggesting that tenecteplase (TNK) the
2
While NIHSS >5 is usually used as the standard for clinically disabling, there are exceptions to this.
For example, a patient presenting with AIHS who demonstrates global aphasia would have a NIHSS of 4.
However, this would be significantly disabling for the patient and therefore, he would likely qualify for
thrombolysis.
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Indications
Clinically disabling AIS (NIHSS>5) with known time of onset ≤4.5hours
BP <185/110mmHg
Blood glucose >50mg/dL
Contraindications
Intracerebral Hemorrhage on CT
Anticoagulation (thrombin or factor Xa inhibtors)
History of intracranial hemorrhage
Ischemic stroke within 3months
Intracerebral neoplasm
Infective endocarditis
Coagulopathy (Platelets 1.7, aPTT >40s, PT>15s)
Table 4 .
Indications and contraindications for tPA [7]. Importantly, the only absolute contraindication to tPA use is
intracerebral hemorrhage on noncontrast CT. The rest are dependent on the clinical scenario.
medication used in thrombolysis for acute myocardial infarctions, is as safe and at
least as effective as tPA [60–62]. The primary advantages to TNK would be its longer
half-life, eliminating the need for a 60minute infusion, and its greater specificity for
fibrin, which could mean more effective thrombolysis [2]. There are currently largescale clinical trials underway to determine the non-inferiority of TNK compared to
tPA (NOR-TEST) and efficacy and safety of TNK in patients presenting more than
4.5hours since LKNT (TIMELESS), and in patients with basilar artery occlusions
(POST-ETERNAL). In the next 10 years, TNK may indeed be the standard of practice.
There are two primary complications that can occur from thrombolysis administration in the acute phase. The first is angioedema and this might occur minutes to
hours after administration of tPA [51]. As mentioned earlier, tPA cleaves plasminogen
into its active form plasmin. Plasmin activates complement as well as the kinin pathways which leads to an inflammatory response and an increase in systemic cytokines.
Therefore, it should not be surprising that one of the consequences of tPA administration is angioedema, an acute albeit transient swelling of deeper layers of the skin and
mucosa. The swelling is red and well-circumscribed and usually involves the orolingual, periorbital, and pharyngeal regions. Angioedema is seen in approximately 5% of
patients who receive tPA and is usually mild and patients who are on ACE inhibitors
are at higher risk [63]. These patients require careful monitoring as if the swelling
becomes severe and involves the airway, the patient may need intubation. Usually the
angioedema is mild and self-resolves after the tPA infusion is complete. The signs and
symptoms of the reaction can be managed by IV diphenhydramine and/or ranitidine
histamine (H1) receptor antagonists [64].
The second major complication of tPA administration, which was alluded to
earlier, is ICH. ICH can occur in up to 7% of tPA administrations and can be associated with up to 83% mortality [65]. Patients must be counseled about this increased
risk to make an informed decision about receiving tPA and clinicians should be aware
of the risk of ICH to recognize and manage it promptly. The factors associated with
a higher risk of ICH include larger volume of hypoperfused tissue, larger established
infarct, higher NIHSS, and higher glucose and/or blood pressure at the time of tPA
Diagnosis and Management of Acute Ischemic Stroke
DOI: http://dx.doi.org/10.5772/.106389
administration [64, 66]. Therefore, patients who receive tPA must have their systolic
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blood pressure kept below 185mmg and be euglycemic. In all patients who receive
tPA, a NCCT should be repeated 24hours post-administration. Even if a patient does
not have a hemorrhage large enough to cause clinical deficits or change in level of
consciousness, the size and location of the ICH will influence future decisions about
secondary stroke prevention. The clinician should have a low threshold to order a stat
repeat NCCT earlier than 24hours if there is a clinical deterioration of the patient.
In summary, tPA is an effective tool in the management of AIS in carefully selected
patients in whom the benefits of thrombolysis outweigh the risk of hemorrhage.
Unfortunately, a significant number of patients present with AIS outside of the
4.5hour window or meeting another contraindication to tPA. In 2015, a new hope of
treatment emerged for these patients.
. Endovascular thrombectomy
While thrombolysis is effective for a select group of patients, it is accompanied
by several limitations. First, given that this is a systemic fibrinolytic medication, it is
accompanied with the risk of bleeding anywhere in the body, especially in the brain.
Second, only select patients qualify for its administration. Third, the rate of recanalization for proximal, large-vessel occlusions (LVOs) is poor, ranging from 13–50%
[2,67]. These are dense clots that are in the major arteries in the brain (the terminus
of the internal carotid artery, the early branches of middle cerebral artery (MCA; M1,
M2), and the basilar artery), even though these occlusions make up at least one-third
of strokes [67] and can cause significant disability.
These three disadvantages are not shared by the endovascular thrombectomy
(EVT) procedure. In this procedure, a patient is taken to interventional neuroradiology
suite, IV contrast is administered to the patient which sequential x-rays of the head
and neck are obtained. An occlusion is localized when it is evident that there an abrupt
Figure 5.
MRI of patient with acute right middle cerebral artery stroke with DWI on the left and FLAIR on the right. In
the DWI image, the white circle marks an area of diffusion restriction indicating acute ischemia. However, there
are minimal to no changes in the corresponding FLAIR image. This indicates that a significant core has not yet
formed yet and mismatch exists.
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halt of contrast filling the artery. A catheter attached to a wire is inserted into the
femoral artery and advanced until it reaches the clot, which can then be aspirated or
retrieved using a stent (Figure ). The first trials to examine the benefit of EVT were
performed in 2013 and did not show the procedure to be clinically efficacious [2]. This
changed with the advent of new methods of imaging and better catheters and in 2015,
the “Multicenter Randomized Clinical Trial of Endovascular Treatment for Acute
Ischemic Stroke in the Netherlands” (MR CLEAN) trial demonstrated that patients
that received EVT within 6 hours of symptom onset were more likely to achieve
functional independence at 3 months (32.6%) compared to those who received placebo
(19.1%) [68]. Other trials confirmed the findings of MR CLEAN and thus emerged
new guidelines for the eligibility for EVT: ) patients ≥ who presented ) within
hours of symptom onset with a ) LVO, a
) NIHSS ≥
and an ) ASPECTS score of CT ≥ on NCCT [7]. With the introduction of CTP,
clinicians could identify core and penumbra in patients with AIS and determine which
patients could still benefit from intervention. In the subsequent AURORA, DEFUSE 3
and DAWN trials, it was determined that EVT could be safe and effective in patients
presenting up to 24hours post symptom onset [69–71]. However, if a patient presents
outside of the initial six-hour window, they must receive a CT perfusion or MRI with
DWI to determine the volume of core infarct that exists and if there is still mismatch;
otherwise it will be impossible to determine if the patient could benefit from the procedure. As mentioned earlier, there are specific CTP criteria that allow a patient to be
eligible for EVT if they present outside of the initial 6 hour window. The MMR must be
greater than 1.8, the penumbra must be greater than 15mL, and the Tmax >10seconds
[41]. The HERMES meta-analysis of five EVT trials found that patients who received
standard of care without EVT had a 14% higher absolute risk of not having a favorable
outcome compared to those who received EVT. There was no significant difference
in symptomatic hemorrhage between groups. Therefore, it is now standard of care to
consider each patient who presents within 24hours with a proximal LVO for EVT [72].
Unfortunately, not all AIS patients are eligible for EVT. The patient must have
a proximal LVO to be accessible by the current clot-retrieval tools. As clots become
more distal, there is a lower likelihood of successful procedure and higher likelihood
of complications. While experienced interventionalists may go after clots in the
basilar artery, anterior cerebral arteries, and distal middle cerebral arteries, there is
little evidence to suggest the efficacy of these procedures. Second, not all AIS patients
have access to EVT. The intervention is only offered at major, tertiary care centers.
While thrombolysis can be done even in remote settings with neurologists guiding
the treatment via “telestroke”, for EVT a patient needs to be transferred, often over
hundreds of kilometers, to obtain the procedure and by the time they reach the EVT
site, there may be no penumbra left [2].
EVT is also accompanied by its own risks [73]. While ICH is more common with
tPA, there is still a risk of hemorrhagic transformation with EVT as causing reperfusion to already infarcted tissue can cause injury, edema, and resulting hemorrhage.
As this is an interventional procedure, there is always the risk of infection or clot
developing at the site of entry. When the interventionalist is trying to access the
occlusion, pieces of the clot can break off and move distally creating occlusions not
accessible by the catheter. In rare cases, arteries can be damaged or even ruptured
from the catheter itself.
Despite the disadvantages to EVT, it remains at the forefront of AIS therapy. The
advent of EVT has revolutionized stroke protocols and care across the world with the
acute stroke window being extended from a mere 4.5 to an entire day.
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Reperfusion advantages Complications with tPA Geographic factors
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Longer clots Full basal ganglia infarction Fast local workflow
Tandem Occlusions Severe hyperglycemia High costs of tPA
Longer times from LKNT Higher age of patient Thrombectomy team
Proximal Occlusions Severe microangiopathy
Reperfusion advantages Delays with EVT Geographic factors
Shorter clots Unfavorable vascular anatomy Prolonged local workflow
Good Collaterals Delays with anesthesia Low costs of tPA
Earlier presentation EVT team not readily
Distal thrombus location
Adapted from Nogueira et al. [].
Table 5.
Factors that would favor EVT alone (top) vs. factors that favor tPA and EVT strategy (bottom).
available
available
Given the advantages of EVT, the question arises of whether patients with LVO
should go straight for EVT or if they would benefit from tPA administration first.
There have been multiple trials that have compared the use of EVT alone to EVT
combined with thrombolysis and have yielded mixed results. The “Multicenter
Randomized Clinical trial of Endovascular treatment for Acute ischemic stroke in the
Netherlands-NO IV” (MR-CLEAN-NO IV) [74] and “Randomized study of endovascular therapy with versus without intravenous tissue plasminogen activator in acute
stroke with ICA and M1 occlusion” (SKIP) trials [75] did not demonstrate noninferiority of EVT alone compared to EVT and tPA whereas the DIRECT MT [76] and
DEVT trials [77] demonstrated that EVT alone was indeed noninferior. The different
results of the studies may have been due to different characteristics of the study population or of the study design itself. For example, in the DEVT trial, the population had
a higher proportion of patients with intracranial atherosclerosis which can change
the benefit obtained with thrombolysis. There is currently not enough evidence to
suggest a strategy of EVT alone for patients presenting with AIS who have LVOs. It is
necessary to determine if there is a particular subgroup that would benefit from EVT
alone [78]. For example, according to DIRECT MT and MR-CLEAN-NOIV, patients
with tandem occlusions (simultaneous blockage of both internal carotid artery and
middle cerebral artery) may benefit from EVT alone. Patients with large ischemic
cores who receive EVT alone may also have decreased likelihood of symptomatic ICH
as per all of the trials except MR-CLEAN-NOIV. At the same time, taking the time to
select these patient subgroups in a clinical scenario may be detrimental to those who
would benefit from both EVT and tPA. Table illustrates the specific factors that
could favor an EVT alone strategy as well as factors that would favor a thrombolysis
and EVT strategy [79]. As per current guidelines, patients presenting with LVO not
meeting the contraindications to thrombolysis should receive thrombolysis as long as
it does not delay the patient receiving EVT (Figures and ) [7].
. Post-acute care
In the acute window, in patients who receive intervention or have a very large
infarct, it is essential to monitor heart rate and blood pressure every 15minutes for
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Figure 6.
Relationship between time of symptom onset to tPA administration to likelihood of symptomatic ICH (blue line;
left axis) and likelihood of good outcome (green line; right axis). As is evident, with increasing time, the risk of
symptomatic ICH increases and the likelihood of good outcome decreases. Importantly, beyond 270minutes there
is still a higher likelihood of ICH but no significant difference in good outcome. *no significant difference between
treatment and placebo. (adapted from Lees et al. [55]).
Figure 7.
Radiograph of proximal M1 occlusion pre (left) and post (right) EVT procedure. An 81year old female presented
with acute left sided weakness and complete neglect of the left side of space. Her CT angiogram demonstrated an
occlusion on the proximal M1 branch of the MCA and she was sent to the interventional neuroradiology suite.
The figure on the left demonstrates no contrast filling the branches of the MCA distal to the clot (arrow). After
thrombectomy, the artery is recanalized and there is anterograde flow (right).
2hours, every 30minutes for 6hours, and every 60minutes until 24hours after starting treatment [80]. It is also pertinent to monitor the patients “neurovitals” their level
of consciousness, strength, and language to ensure their clinical status is not deteriorating. As previously discussed, there should be a low threshold for repeating a NCCT
in the acute period. Patients with AIS should also be kept NPO until their swallowing
is assessed formally as their decreased level of consciousness and facial weakness can
increase the likelihood of aspiration. All stroke patients who receive tPA, EVT, or who
present with significant deficits, should be admitted to a dedicated stroke unit where
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